This invention relates to a method of blocking or reversing peripheral vasoconstriction, more specifically, to a method of treating peripheral vasoconstriction by the administration of an antiestrogenic agent such as tamoxifen citrate.
It is well known in the practice of medicine that adrenergic agents, notably epinephrine, norepinephrine and dopamine, are potent vasoconstrictors. Extreme caution is used when or if such agents are injected into peripheral tissue such as toes, fingers, ear lobes, the nose or the penis. Due to the profound vasoconstrictive effect of the adrenergic agents, intentional or unintentional injection of an adrenergic agent into peripheral tissue can lead to vasoconstriction, loss of blood flow, and tissue necrosis. In extreme cases, loss of blood flow due to the vasoconstriction may result in amputation of the toe, finger or other body part. It would be advantageous, therefore, to provide a method of blocking or reversing the vasoconstrictive effect of a potent vasoconstrictor by the administration of a readily available, oral, pharmcological agent, such as an antiestrogenic steroid.
It is known that the epinephrine content of the spleen, heart and uterus of rats is increased after the administration of estrogens. Furthermore, it is known that there is an increase in adrenergic nerve terminals and neurotransmitter content in female genital organs caused by estrogen treatment. That sex hormones may play a role in blood flow regulation in the uterus is not unexpected. Furthermore, it has been previously demonstrated, that antiestrogens, such as tamoxifen, have an effect on the development of renal cortical necrosis induced by estrogen plus vasopression. Antiestrogen induced alteration of hypothalmic dopamine and norepinephine levels in rats has also been demonstrated. Moreover, it has been shown that the antiestrogen tamoxifen is a calcium antagonist in perfused rat mesentary. Heretofore, however, no one has taught or suggested the use of an antiestrogen, such as tamoxifen citrate to modify the vasoactive effects of an exogenous adrenergic agent on peripheral blood flow.